No time to waste: decreasing patient wait times for chemotherapy administration using automated prioritization in an oncology pharmacy system.

OBJECTIVES: To implement an automated pharmacy dispensing prioritization system and to evaluate its effect on the timing of dispensing and administration of chemotherapy. STUDY DESIGN: An electronic chemotherapy dispensing system that prioritized orders for pharmacy processing based on anticipated patient arrival at the oncology outpatient unit was implemented, followed by an educational intervention for pharmacy staff. METHODS: A time-controlled study evaluating the effect of the electronic chemotherapy dispensing system on late, early, and "within target" dispensing and administration of chemotherapy was conducted. RESULTS: A total of 13,138 chemotherapies were prepared and released pending medical clearance based on laboratory results (hereafter referred to as pending counts) (8677 [66.0%]) or pending arrival of the patient (hereafter referred to as pending arrival) (4461 [34.0%]) from March 1, 2005, to March 2, 2006. Chemotherapy dispensing and administration times were retrospectively compared with chemotherapy appointment times after adjustment for late patient arrival. Dispensing times continuously decreased from a mean delay in dispensing of 12 minutes after the adjusted chemotherapy appointment time at baseline to dispensing a mean of 5 minutes ahead of the scheduled time by the end of the study. Chemotherapy treatments dispensed within target increased from 62.9% to 74.7% (pending arrival) and from 53.4% to 68.1% (pending counts), and those administered within target increased from 64.9% to 71.8% (pending arrival) and from 56.0% to 70.1% (pending counts). CONCLUSION: An automated intervention for synchronizing chemotherapy preparation with anticipated times for administration was associated with significant reduction in wait times.

Growth factors and chemotherapeutic modulation of breast cancer cells.

A variety of molecules including growth factors are involved in the metastasis of breast cancer cells to bone. We have investigated the effects of osteoblast derived growth factors, such as insulin-like growth factor-1 (IGF-1) and transforming growth factor beta-1 (TGF-beta1), on doxorubicin (adriamycin)-induced apoptosis and growth arrest of estrogen receptor positive (ER+) (MCF-7) and negative (ER-) (MDA-MB-435) breast cancer cell lines. Human breast normal epithelial (MCF-10A), breast cancer (MCF-7) and metastatic breast cancer (MDA-MB-435) cell lines were exposed to different doses of doxorubicin (0.1, 1 or 10 microM) at various exposure times (12, 24 or 48 h). The doxorubicin cytotoxicity was found to be higher in cancer cell lines (MDA-MB-435 and MCF-7) compared with normal breast epithelial cells (MCF-10A cells). Doxorubicin appeared to exert a blockade of MCF-7 and MDA-MB-435 cells at the G2/M phase, and induced apoptosis in MDA-MB-435 (29 +/- 4.2% vs 3.4 +/- 1.9% control) as assessed by flow cytometry, DNA fragmentation and terminal deoxynucleotidyl-transferase mediated deoxyuridine 5-triphosphate and biotin nick-end labelling (TUNEL) assays. Estradiol (E2) stimulated the growth of MCF-7 cells and increased the distribution of the cells at the G2/M and S phases. Exogenous IGF-1 partially neutralized the doxorubicin cytotoxicity in both cancer cell lines (MCF-7 and MDA-MB-435). Similarly, TGF-beta1 partially neutralized the doxorubicin cytotoxicity in MDA-MB-435 cells by reducing the number of cells at the